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Case Report
Very Late Bare-Metal Stent Thrombosis. A Case Report and Review of the Literature
July 2006
Stent thrombosis is defined as acute thrombotic occlusion in the stented segment of a coronary artery, usually presenting as ST-segment elevation myocardial infarction,1 and typically occurs within the first several weeks after stent placement. Stent thrombosis has traditionally been categorized as either subacute stent thrombosis (SAT), occurring within 30 days, or as late stent thrombosis (LST), occurring beyond 30 days.2 While very late stent thrombosis (VLST), occurring beyond 1 year, has been increasingly described with the use of drug-eluting stents,3,4 thrombosis this late with bare-metal stents is very uncommon. We report a case of very late thrombosis of a bare-metal stent occurring 717 days after implantation.
Case Report. A 71-year-old African-American male with a past medical history of hypertension and hypercholesterolemia was brought to the hospital via ambulance for acute-onset chest pain with nausea on July 7, 2005. His past medical history included a percutaneous coronary intervention (PCI) in June 2003, with the placement of 2 bare-metal stents in the proximal right coronary artery (RCA) (Express 4 x 8 mm at 18 atm, 4 x 12 mm at 16 atmospheres) and 1 bare-metal Express™ stent (Boston Scientific Corp., Natick, Massachusetts) in the mid-RCA (3.5 x 8 mm at 18 atm). After the procedure, the patient was completely asymptomatic (with good exercise tolerance) and did not undergo any further cardiac testing. His current medications included only metoprolol and aspirin. He had been taking clopidogrel (75 mg /day) for the initial 3 months post-stent implantation, and was only intermittently compliant with aspirin since that time. His electrocardiogram on admission revealed > 2 mm ST-segment elevations in leads II, III and aVf, and ST-depressions in aVL, and V2–V6 (Figure 1). The patient was given aspirin 325 mg and clopidogrel 300 mg in the emergency room. He was also started on tirofiban and heparin infusions and was immediately transferred to the cardiac catheterization laboratory. Coronary angiography revealed a thrombotic occlusion of the previously stented segment of the proximal RCA, without any major retrograde collaterals from the left coronary system (Figure 2). Left ventriculography revealed posterobasal hypokinesia and an ejection fraction of 55%. There was no evidence of mitral regurgitation. The total occlusion was easily crossed with the use of a floppy guidewire, and the lesion was predilated with a 3.0 x 15 mm Maverick® balloon (Boston Scientific) at 8 atm. Partial antegrade flow was established with some residual thrombus overlying the stented segment of the proximal RCA (Figure 3). Distal embolization of the thrombus was noticed in the posterior descending artery (PDA) and a posterolateral branch. An Express bare-metal stent was then implanted (3.5 x 24 mm at 20 atm) with an excellent angiographic result (Figure 4), followed by resolution of the patient’s chest pain and ST-segment elevations on ECG. The patient was discharged from the hospital 2 days later with standard medical regimen including clopidogrel for 1 year and aspirin indefinitely, given his history of stent thrombosis.
Discussion and Review of the Literature. Coronary stenting has revolutionized the practice of interventional cardiology. It has dramatically improved upon the acute procedural success and also reduced the restenosis rates observed with balloon angioplasty alone.5–7 Despite these advantages, stent thrombosis was a new problem associated with the procedure, occurring in up to 4.7% of cases in the early series.8 Fortunately, stent thrombosis has in large part been overcome by the use of high-pressure inflation and dual antiplatelet therapy, consisting of aspirin and a thienopyridine.9–11 It has been demonstrated that the aggressive use of antiplatelet agents such as aspirin and either ticlopidine or clopidogrel decreased the incidence of early and late stent thrombosis to less than 1%.10–12 In the recently published TAXUS V trial, the incidence of stent thrombosis in the bare-metal arm of the study group was 0.5% at 30 days, 0.2% at 6 months and 0% at 9 months.13 There have been no studies looking specifically at the determinants and incidence of VLST (i.e., occurring beyond 1 year) with the use of bare-metal stents. While VLST is increasingly being recognized as a complication of drug-eluting stents where it may be related to delayed endothelialization,2–4,14 it is distinctly uncommon with the use of bare-metal stents outside the context of brachytherapy.15–17 We were able to find only 3 published series reporting on a total of 5 cases18,22,23 of late stent thrombosis occurring with the use of bare-metal stents (Table 1). All of these cases had the stent thrombosis occurring in either the LAD or the RCA, with none in the left circumflex artery. The duration between the initial stent placement and the subsequent thrombotic event ranged from 420 and 930 days. Three of the patients in these reports were not taking a thienopyridine at the time of the thrombotic event, while in the other 2 patients, there was no documentation of its use. Two patients were still on aspirin, although their compliance was questionable. In the other 3 patients, there was no documentation as to whether they were taking aspirin. In our patient, the time to the acute thrombotic event from the index PCI was 717 days. We could not identify any potential explanations for this acute event in our patient except for the possibility that he had only been intermittently compliant with aspirin. In addition, he had initially received 2 overlapping stents in 2003 that may have been underexpanded. However, since IVUS was not performed during the acute event, this suspicion could not be confirmed.
Presumed causes of bare-metal stent thrombosis, both early and late, include noncompliance with antiplatelet agents,15 exercise-induced procoagulant state,16 brachytherapy,17 small stent size and underdeployment of the stent.18 Impaired response to antiplatelet therapy has also been reported,19,20 and may indeed represent a potential mechanism in our patient. Since there is no published literature on the specific causes of VLST, it is conceivable and probable that many of the same mechanisms that lead to SAT and LST may also be responsible for VLST. The role of IVUS in investigating the possible pathophysiological mechanisms is very important and cannot be underestimated.21
The management of VLST is similar to that of SAT and LST, and consists of the restoration of perfusion to TIMI grade 3 — most commonly by a variety of percutaneous techniques such as balloon angioplasty, AngioJet® (Possis Medical, Inc., Minneapolis, Minnesota) thrombectomy, or re-stenting with subsequent long-term (if not lifelong) dual antiplatelet therapy. However, these patients are at higher risk for recurrent thrombosis.22Conclusion. Very late stent thrombosis with the use of bare-metal stents, although fortunately infrequent, is a catastrophic event. While VLST is very rare with the use of bare-metal stents, it is increasingly being recognized with the growing use of drug-eluting stents, where the mechanisms are incompletely understood and likely different than those for bare-metal stents. The optimum duration of antiplatelet therapy for patients with coronary artery stents still remains to be determined. Most importantly, education regarding the importance of compliance with combination antiplatelet therapy needs to be emphasized. In addition, avoidance of stent undersizing by the operator and adequate high-pressure inflations during deployment are technical considerations that are critical if this complication is to be avoided.
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